Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are associated with a modest but significant increase in serum magnesium levels. This report describes improvement in serum magnesium and associated symptoms after initiating SGLT2i therapy in a patient with refractory hypomagnesemia. A 58-year-old woman presented with persistent hypomagnesemia refractory to oral magnesium supplements. She had history of type 2 diabetes mellitus, hypothyroidism, fibromyalgia, and degenerative disk disease. The cause of hypomagnesemia was attributed to excessive renal losses. Laboratory investigations revealed serum magnesium of 1.2 mg/dL with fractional excretion of magnesium (FEMg) of 8.9%. She was started on Empagliflozin 10 mg daily. Within 4 weeks of therapy, her serum magnesium level corrected with symptomatic improvement, which was sustained a few weeks later. Subsequently, her oral magnesium supplements dose was reduced. SGLT2i has been shown to improve magnesium levels in patients with urinary magnesium wasting. Several mechanisms have been postulated but the exact physiology remains unknown. SGLT2i have been efficacious for glycemic control, renal protection, decreasing the risk of ASCVD events, and cardiac mortality in patients with diabetes. In addition, renal and cardiac benefits are also demonstrated in patients without diabetes. This observation demonstrates that SGLT2i can improve the management of patients with otherwise intractable hypomagnesemia.
INTRODUCTION Drug-induced immune thrombocytopenia (DITP) is a rare and often difficult-to-diagnose cause of thrombocytopenia, caused by drug-dependent platelet antibodies leading to increased platelet consumption and destruction. DITP evolves within 7 days of initiation of the offending drug and is characterized by thrombocytopenia, with or without bleeding manifestations. Immediate discontinuation of the inciting drug remains the cornerstone of management. Although the most commonly identified drugs are quinine, penicillamine, and valproic acid, isolated cases of ceftriaxone-induced immune thrombocytopenia have been reported. CASE REPORT A 60-year-old female presented with fever, dysuria, and fatigue for 3 days with associated proximal muscle weakness for a few weeks. She was diagnosed with right pyelonephritis with urine cultures growing non-ESBL (extended-spectrum beta-lactamase) Escherichia Coli for which she was started on Ceftriaxone 2g daily. She was also started on low-dose prednisone 20mg daily for fibromyalgia. Her platelet count continued to downtrend and on day 7 of treatment reached a nadir of 18K/μL. Heparin-induced thrombocytopenia (HIT) was excluded. She received one unit of platelets and ceftriaxone was switched to ceftazidime, with which her platelet counts improved. Owing to the temporal relationship between the development and resolution of thrombocytopenia with the commencement and withdrawal of ceftriaxone, drug-induced thrombocytopenia was diagnosed. Naranjo's algorithm revealed a probable adverse drug reaction but confirmatory tests for ceftriaxone-induced platelet antibodies could not be performed. DISCUSSION DITP remains a diagnosis of exclusion and poses a significant therapeutic challenge. Clinicians need to have a high index of suspicion to rule out common causes of unexplained thrombocytopenia before diagnosing DITP.
Drug-induced pancreatitis is a rare and sometimes fatal cause of pancreatitis which is often difficult to diagnose. Acid suppressing medications include histamine-2 receptor antagonists and proton pump inhibitors have been linked to acute pancreatitis in several case-reports and recent systematic reviews. However, only one case of lansoprazole induced pancreatitis has been described in literature until date. A 67-year-old female presented with complaints of abdominal pain, nausea, vomiting and worsening generalized weakness for the past 1 week. She had recently been started on lansoprazole therapy for gastroesophageal reflux with no other change in medications. She denied any trauma, recent viral infection, alcohol intake, over-the-counter or herbal medication use. On presentation, she had abdominal distension with tenderness and epigastric guarding. Laboratory investigations were significant for leukocytosis and elevated amylase and lipase with normal triglyceride levels. Computed tomography of the abdomen and pelvis with contrast revealed features of acute interstitial pancreatitis with retroperitoneal lymphadenopathy and no other abnormality. She was diagnosed to have acute pancreatitis secondary to lansoprazole therapy and was managed conservatively. Her symptoms resolved after 3 days of discontinuation of the drug. There have been several cases reporting a potential link between acute pancreatitis and acid suppressing medications. However, drug-induced pancreatitis still remains a diagnosis of exclusion as it is difficult to establish causality. Almost all the acid suppressing medications have been linked to pancreatitis, but a case associated with lansoprazole has only been described once. Further studies are needed to establish causation.
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